Cited by 245Gut microbiota and healthImmune Response and InflammationProbiotics and Fermented Foods

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Interactions Between the Gut Microbiota and the Host Innate Immune Response Against Pathogens

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Cheng, Hong-Yu, Ning, Meng-Xia, Chen, De-Kun, Ma, Wen-Tao·2019·Frontiers in Immunology

Abstract

The mammalian intestine is colonized by over a trillion microbes that comprise the "gut microbiota," a microbial community which has co-evolved with the host to form a mutually beneficial relationship. Accumulating evidence indicates that the gut microbiota participates in immune system maturation and also plays a central role in host defense against pathogens. Here we review some of the mechanisms employed by the gut microbiota to boost the innate immune response against pathogens present on epithelial mucosal surfaces. Antimicrobial peptide secretion, inflammasome activation and induction of host IL-22, IL-17, and IL-10 production are the most commonly observed strategies employed by the gut microbiota for host anti-pathogen defense. Taken together, the body of evidence suggests that the host gut microbiota can elicit innate immunity against pathogens.

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Crossref · 10.3389/fimmu.2019.00607

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Figure 1 Gut microbiota plays an important role in the induction of antimicrobial peptides expression against pathogens. Antimicrobial peptides are key components of innate immunity to control pathogen growth within the intestine. Accumulated evidence identified that gut microbiota can contribute to the expression of antimicrobial peptides and play a central role in host defense against pathogens. Paneth cells could directly sense gut microbiota through cell-autonomous myeloid differentiation primary response 88 (MyD88)-dependent toll-like receptor (TLR) activation, triggering expression of α-defensins and C-type lectins. With regard to β-defensin, gut microbiota induce β-defensin expression in cell culture mediated by NF-κB- and MAPK/AP-1-dependent pathways in vitro. Then β-defensin interacts with intestinal epithelial cell (IEC) through CCR6 to activate epithelial restitution and barrier repair.
Figure 1 Gut microbiota plays an important role in the induction of antimicrobial peptides expression against pathogens. Antimicrobial peptides are key components of innate immunity to control pathogen growth within the intestine. Accumulated evidence identified that gut microbiota can contribute to the expression of antimicrobial peptides and play a central role in host defense against pathogens. Paneth cells could directly sense gut microbiota through cell-autonomous myeloid differentiation primary response 88 (MyD88)-dependent toll-like receptor (TLR) activation, triggering expression of α-defensins and C-type lectins. With regard to β-defensin, gut microbiota induce β-defensin expression in cell culture mediated by NF-κB- and MAPK/AP-1-dependent pathways in vitro. Then β-defensin interacts with intestinal epithelial cell (IEC) through CCR6 to activate epithelial restitution and barrier repair.CC BY · PubMed Central
Figure 2 Gut microbiota enhance the expression of IL-22 against invading pathogens. IL-22 is important in maintaining the integrity of mucosal barriers and can be produced by many different types innate immune cells, which induce the expression of various antimicrobial proteins, including lipocalin-2, calprotectin, C-type lectins, S100A8, S100A9, and so on to clear pathogens. Increasing evidence identified that gut microbiota enhances the expression of IL-22 to protect the host against pathogens. The results show that gut microbiota utilize tryptophan as an energy source and produce a metabolite, indole-3-aldehyde (IAld), which in turns activated Ahr on innate immune cells. Once activated, innate immune cells will secrete IL-22, which protects the host against opportunistic pathogens by reducing their colonization.
Figure 2 Gut microbiota enhance the expression of IL-22 against invading pathogens. IL-22 is important in maintaining the integrity of mucosal barriers and can be produced by many different types innate immune cells, which induce the expression of various antimicrobial proteins, including lipocalin-2, calprotectin, C-type lectins, S100A8, S100A9, and so on to clear pathogens. Increasing evidence identified that gut microbiota enhances the expression of IL-22 to protect the host against pathogens. The results show that gut microbiota utilize tryptophan as an energy source and produce a metabolite, indole-3-aldehyde (IAld), which in turns activated Ahr on innate immune cells. Once activated, innate immune cells will secrete IL-22, which protects the host against opportunistic pathogens by reducing their colonization.CC BY · PubMed Central

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Metadata

Authors
Cheng, H.-Y., Ning, M.-X., Chen, D.-K., & Ma, W.-T.
Affiliations
Northwest A&F University (CN)
Venue
Frontiers in Immunology
Published
2019-03-29
Volume
10
Pages
607-607
ISSN
1664-3224 (ISSN-L)
OpenAlex
W2926238016
Cited by
244
References
150
Citations by year
2026: 16 · 2025: 39 · 2024: 51 · 2023: 35 · 2022: 38 · 2021: 38 · 2020: 22 · 2019: 4
FWCI
2.25
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Northwest Agriculture and Forestry University (00500/Z109021716)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
Keywords
gut microbiota, innate immunity, host-pathogen interaction, intestinal epithelium, antimicrobial peptides, inflammasome activation, IL-22, IL-17, IL-10, mucosal immunity, immune system maturation
MeSH terms
Gastrointestinal Microbiome, Animals, Humans, Immunity, Innate, Intestinal Mucosa, Cytokines, Antimicrobial Cationic Peptides, Inflammasomes

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